Inhalation of chrysotile asbestos causes neoplastic and fibrotic lung disease. In humans it is known that exposure to asbestos dust in both occupational and environmental settings leads to a slowly progressing, interstitial lung disease. The pulmonary lesions are characterized by diffuse fibrosis which is most prominent at bronchiolar-alveolar junctions. We have established the initial deposition sites and translocation pathways of inhaled asbestos. We have presented an intracellular actin-mediated contractile mechanism by which particles are moved through the alveolar epithelium to the interstitium. In addition, an early interstitial lesion (microcalcification) has been demonstrated within alveolar duct bifurcations where asbestos fibers were deposited initially. Epithelial, macrophage and interstitial cell interactions with asbestos lead to progressive alterations in cell number, volume and production of connective tissue components as determined by ultrastructural morphometric techniques.